tbuckley/cabot-search huggingface dataset:
Stroke mortality declines; still major health problem
Authors: P. Gunby
Journal: JAMA (1984)

Although cerebrovascular disease remains a major health problem in the United States and elsewhere, "the death rate from stroke declined by 46% from 1968 to 1981," an American Heart Association (AHA) official—Edward S. Cooper, MD—points out. Cooper, who is professor of medicine, University of Pennsylvania School of Medicine, Philadelphia, is chair of the AHA's Stroke Council. He noted during the AHA's annual scientific sessions in Anaheim, Calif, that "the rate of death from all diseases in the United States dropped by only 13%" while a larger decline in stroke-related deaths was being documented. And, says a researcher at the Center for Demographic Studies, Duke University, Durham, NC, "recent data suggest that this trend [the declining mortality rate associated with stroke] is continuing." Kenneth G. Manton, PhD, an associate research professor at the center, has been working with the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS), Bethesda, Md,
Falls
Authors: Steven R. Cummings, Michael C. Nevitt
Journal: New England Journal of Medicine (1994)

Nearly one third of people 65 years of age or older fall each year. This risk increases with age and is much higher among persons living in long-term care institutions than among those in the community1. From 10 to 15 percent of falls result in serious injuries, at least half of which are fractures2,3. In white women, only 1 percent of falls result in hip fractures, but such fractures account for a large share of the disability, death, and medical costs associated with falls. Falls can break self-confidence as well as bones: up to a quarter of . . .
Diabetes Mellitus and Its Degenerative Complications: A Prospective Study of 4,400 Patients Observed Between 1947 and 1973
Authors: Jean Pirart
Journal: Diabetes Care (1978)

This article was originally published in French in Diabete et Metabolisme (vol. 3: 97–107, 173–182, 245–256; 1977). The Editors of DIABETES CARE thank the author, and the editors and publisher of Diabete et Metabolisme for granting permission for us to print this English translation. The paper was translated by Marjorie Levin of Miami, Florida. Part I of this translation appeared in the May–June issue of DIABETES CARE (vol. I: 168–188).
Tuberculosis Outbreak Among HIV-Infected Persons
Journal: JAMA (1991)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Superoxide is involved in the pathogenesis of paraquat-induced injury in cultured rat liver slices
Authors: Hitoshi Togashi, Haruhide Shinzawa, Hiroto Wakabayashi, Toichiro Nakamura, Huang Yong, Nobuo Yamada, Katsuaki Ukai, Yoshimi Okuyama, Tsuneo Takahashi, Makoto Ishikawa
Journal: Hepatology (1991)

We examined whether superoxide is a factor responsible for paraquat-induced liver injury in terms of superoxide dismutase using cultured rat liver slices exposed to various concentrations of paraquat. The degree of liver injury was assessed by measurement of percentage of lactate dehydrogenase leakage into the medium and lipid hydroperoxides in the liver slices and by direct histopathological observation. Paraquat produced concentration- and time-related liver injury in the cultured rat liver slices. Notably, after exposure to 5 mmol/L paraquat, a significant increase of the percentage of lactate dehydrogenase leakage occurred from 4 hr (p &lt; 0.05 vs. control group), and this gradually increased up to 8 hr (p &lt; 0.01 and p &lt; 0.001 vs. control group at 6 and 8 hr, respectively). Changes in lipid hydroperoxides in the liver slices were similar to those in percentage of lactate dehydrogenase leakage (p &lt; 0.05 and p &lt; 0.01 vs. control group at 6 and 8 hr, respectively). Liver injury was located around the central vein at 6 hr and gradually spread at 8 hr. Paraquat-induced liver injury was aggravated both biochemically and histopathologically by pretreatment with 5 mmol/L diethyldithiocarbamate, an inhibitor of copper- and zinc-containing superoxide dismutase activity (percentage of lactate dehydrogenase leakage: p &lt; 0.01 and p &lt; 0.001 vs. paraquat group at 6 and 8 hr, respectively; lipid hydroperoxides: p &lt; 0.01 vs. paraquat group at 8 hr). Incubation of liver slices with liposome-encapsulated superoxide dismutase increased the augmentation of superoxide dismutase in the liver slices. Paraquat-induced liver injury was attenuated both biochemically and histopathologically by addition of an identical concentration of liposome-encapsulated superoxide dismutase (100 U/ml) (percentage of lactate dehydrogenase leakage: p &lt; 0.01 and p &lt; 0.01 vs. paraquat group at 6 and 8 hr, respectively; lipid hydroperoxides: p &lt; 0.05 and p &lt; 0.01 vs. paraquat group at 6 and 8 hr, respectively). However, the same concentration of free superoxide dismutase as that included in superoxide dismutase in liposome-encapsulated superoxide dismutase showed neither augmentation of superoxide dismutase in the liver slices nor hepatoprotection. These results suggest that superoxide is involved in the pathogenesis of paraquat-induced liver injury. (Hepatology 1990;14:707-714.)
THE FIRST FRENCH PUBLICIST—A BIT OF MEDICAL HISTORY.
Journal: JAMA (1906)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Current attempts to prevent the use of animals in medical research
Authors: M. B. Visscher
Journal: JAMA (1981)

THE CURRENT strategy of the animal welfare and antivivisection groups in the United States is to assert that the use of living vertebrate animals in research is not essential to progress in medical science. Their lobbying activities have induced some 50 members of Congress to introduce or cosponsor one of four bills in the House of Representatives, to promote so-called alternative methods to the use of living animals in medical research and toxicity testing. The most strongly supported bill is HR 4805, called the Research Modernization Act. Another measure that has very strong animal humane society support is HR 6847, "to amend the Animal Welfare Act to insure the humane treatment of laboratory animals." Both bills would impede scientific research. These bills, which did not pass in the 96th Congress, will probably be introduced in the 97th Congress with new numbers. The scientific and medical communities should be alerted to
THE CAUSES OF THE CACHEXIA ACCOMPANYING MALIGNANT TUMORS.
Journal: JAMA (1904)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Carcinogenicity of 1,3-Butadiene
Authors: Ronald L. Melnick, Cynthia C. Shackelford, James Huff
Journal: Environmental Health Perspectives (1993)

1,3-Butadiene, a high-production volume chemical used largely in the manufacture of synthetic rubber, is a multiple organ carcinogen in rats and mice. In inhalation studies conducted in mice by the National Toxicology Program, high rates of early lethal lymphomas occurring at exposure levels of 625 ppm or higher reduced the development and expression of later developing tumors at other sites. Use of survival-adjusted tumor rates to account for competing risk factors provided a clearer indication of the dose responses for 1,3-butadiene-induced neoplasms. An increase in lung tumors in female mice was observed at exposure concentrations as low as 6.25 ppm, the lowest concentration ever used in a long-term carcinogenicity study of this gas. Human exposures to 1,3-butadiene by workers employed at facilities that produce this chemical and at facilities that produce styrene-butadiene rubber have been measured at levels higher than those that cause cancer in animals. Furthermore, epidemiology studies have consistently revealed associations between occupational exposure to 1,3-butadiene and excess mortality due to lymphatic and hematopoietic cancers. In response to the carcinogenicity findings for 1,3-butadiene in animals and in humans, the Occupational Safety and Health Administration has proposed lowering the occupational exposure standard for this chemical from 1000 ppm to 2 ppm. Future work is needed to understand the mechanisms of tumor induction by 1,3-butadiene; however, the pursuit of this research should not delay the reduction of human exposure to this chemical.
THE ANTITOXIN OF DIPHTHERIA AT NEW YORK CITY—COST OF PLANT.
Journal: JAMA (1894)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
From the Centers for Disease Control. Pneumonic plague--Arizona, 1992
Journal: JAMA (1992)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
The Dietary Fat—Breast Cancer Hypothesis: Is It Really Alive?-Reply
Authors: Arthur Schatzkin
Journal: JAMA (1990)

<h3>In Reply.—</h3> Dr Evans suggests that estrogenic contaminants of fat in certain meat products may be involved in the etiology of breast cancer. While this notion is biologically plausible, it by no means rules out a role for dietary fat per se. We cited both animal and ecological (international correlation, time trend, and migration) data in support of the dietary fat—breast cancer hypothesis. Residual estrogens in US meat products cannot satisfactorily account for these data. We agree with Drs Klurfeld and Kritchevsky that animal experiments clearly show that energy restriction reduces breast tumorigenesis in rodent models. However, it is not the case, as Drs Klurfeld and Kritchevsky imply, that the tumor-reducing effect of low fat in animal experiments is wholly attributable to reduced total energy intake. Animal studies of mammary carcinogenesis, carefully considered in toto, do demonstrate a fat effect independent of total energy intake.<sup>1</sup>, It is interesting that
First Certifying Examination of the American Board of Laser Surgery
Journal: JNCI Journal of the National Cancer Institute (1986)

Journal Article First Certifying Examination of the American Board of Laser Surgery Get access JNCI: Journal of the National Cancer Institute, Volume 77, Issue 3, September 1986, Page 835, https://doi.org/10.1093/jnci/77.3.835-c Published: 01 September 1986
Expression of multidrug resistance genes in rat liver during regeneration and after carbon tetrachloride intoxication
Authors: H Nakatsukasa
Journal: Hepatology (1993)

We analyzed expression of multidrug resistance (mdr) genes in rat liver during regeneration after partial hepatectomy or carbon tetrachloride–induced necrosis. In situ hybridization revealed that in the normal liver the cellular distribution of mdr transcripts and protein is restricted to hepatocytes and that a gradient, highest in zone 1 and lowest in zone 3, exists in the level of the mdr transcripts in the liver acinus. Increased levels of mdr1a and mdr1b transcripts were observed 3 hr after administration of carbon tetrachloride and remained increased for the next 5 days. In contrast, increased expression of mdr1a and mdr1b was first observed 24 hr after partial hepatectomy. Use of gene-specific probes to compare the time courses of mdr1b and mdr2 expression after carbon tetrachloride administration showed distinctly different patterns of expression; mdr1b reached a maximum level of expression at 12 hr, whereas increased mdr2 expression was first observed 48 hr after administration. Nuclear run-on analysis at 12 and 24 hr after carbon tetrachloride administration demonstrated 10-fold and eightfold increases in mdr transcription, respectively. However, 72 hr after carbon tetrachloride treatment the rate of mdr transcription was back to the control level. The cellular patterns of mdr expression after partial hepatectomy and carbon tetrachloride administration were similar; the increase was first observed in zone 1 and gradually extended into zone 3. These data strongly suggest that the physiological roles of mdr1b and mdr2 are different and that liver regeneration is an appropriate model for elucidating these differences. (HEPATOLOGY 1993;18:1202-1207).
Managing comorbidities in oncology: A multisite randomized controlled trial of continuing versus discontinuing statins in the setting of life-limiting illness.
Authors: Amy Pickar Abernethy, Jean Kutner, Patrick Jud Blatchford, Christine Ritchie, Diane Fairclough, Laura Hanson, Janet Bull
Journal: Journal of Clinical Oncology (2014)

LBA9514 Background: For patients with life-threatening illness such as advanced cancer, optimal management of longstanding medications prescribed for comorbid illness is uncertain. Risks may outweigh benefits; e.g., benefits from HMG Co-A reductase inhibitors (“statins”) may take years to accrue and may not be relevant for a person with limited prognosis. Is it safe to discontinue statins for the patient with less than a year to live? Methods: This was a multicenter, unblinded pragmatic trial. At enrollment, participants were randomized (1:1) to discontinue or continue their statin medication. Eligible patients were adults with advanced life-limiting illness on a statin for ≥3 months for primary or secondary prevention, a life expectancy of greater than one month, and evidence of recent deterioration in performance status. Outcomes measured at baseline and at least monthly included survival, cardiovascular-related events, quality of life (QOL), symptoms, and polypharmacy. Rate of death within 60 days of randomization was the primary outcome. Results: 381 patients were enrolled (189 discontinue statins; 192 continue statins). Mean age was 74 years (SD 12); 22% were cognitively impaired; 49% had cancer as the primary diagnosis; and, 69% had used statins for >5 years. Rate of death within 60 days was not statistically different between groups (discontinue vs. continue, 23.8% vs. 20.3%, 90% CI -3.5% to 10.5%, p=0.36). The group discontinuing statins had longer median time-to-death (229 days [90% CI 186–332] vs. 190 days [90% CI 170-257]; p=0.60). Total QOL was significantly better among the group discontinuing statins (McGill QOL: 7.11 vs. 6.85, p=0.037) and there were fewer symptoms in this group (Edmonton Symptom Assessment Scale: 25.2 vs. 27.4, p=0.128). People in the discontinue statins group took significantly fewer medications (10.1 vs. 10.8, p = 0.034). Few participants in either group experienced cardiovascular events (13 vs. 11). Conclusions: In the setting of life-limiting illness such as advanced cancer, it is unlikely that harm will accrue when statins being used for primary or secondary prevention are discontinued; these patients may even benefit. Clinical trial information: NCT01415934.
Winds of Change: Reducing Transboundary Air Pollutants
Authors: Christopher G. Reuther
Journal: Environmental Health Perspectives (2000)

Sulfur dioxide, nitrogen oxides, volatile organic compounds, persistent organic pollutants, particulate matter, and heavy metals---air pollutants once thought to be problems that could be solved locally, where the effects occur---are all currently being discussed in international forums. A spate of meetings and agreements in recent months has shown many international governments to be more willing than ever to try to limit the amount of their air pollution that drifts into other countries. Prompting this policy shift are increasing emissions in some parts of the world, better monitoring, and an improved understanding of air pollution transport and the effects of air pollution. In most regions of the world, however, no international agreements on air pollution exist at all, while in others, many overlapping local, multilateral, and global agreements address the problem simultaneously. According to the World Health Organization, air pollution causes nearly 3 million deaths per year, and the U.S. Environmental Protection Agency estimates that ground-level ozone causes damage to U.S. crops totaling $1-2 billion each year.
PHYSICAL DIAGNOSIS: REQUIEM OR RENAISSANCE?
Journal: JAMA (1965)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
The Solitary Nodule (Coin Lesion) of the Lung
Journal: JAMA (1963)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal